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Cell Signaling Technology
Pim-3 (D17C9) Rabbit Monoclonal Antibody
#4165 · $149
100
Citing papers
13.8k
Combined citations
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Research areas
Cytokine Signaling Pathways and Interactions
14
Cellular Mechanics and Interactions
6
Immune Response and Inflammation
6
Signaling Pathways in Disease
6
Metabolism, Diabetes, and Cancer
5
Cancer, Hypoxia, and Metabolism
5
Cancer Mechanisms and Therapy
5
DNA Repair Mechanisms
5
Papers citing this product
1
Systemic Treatment with the Antidiabetic Drug Metformin Selectively Impairs p53-Deficient Tumor Cell Growth
Cancer Research
·
2007
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917 cit.
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DOI
2
Microvesicles secreted by macrophages shuttle invasion-potentiating microRNAs into breast cancer cells
Molecular Cancer
·
2011
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699 cit.
·
DOI
3
RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome
Nature Communications
·
2017
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596 cit.
·
DOI
4
Human CtIP Mediates Cell Cycle Control of DNA End Resection and Double Strand Break Repair
Journal of Biological Chemistry
·
2009
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507 cit.
·
DOI
5
Expression of transketolase TKTL1 predicts colon and urothelial cancer patient survival: Warburg effect reinterpreted
British Journal of Cancer
·
2006
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262 cit.
·
DOI
6
Role of Gas6 receptors in platelet signaling during thrombus stabilization and implications for antithrombotic therapy
Journal of Clinical Investigation
·
2005
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259 cit.
·
DOI
7
The Interaction of CtIP and Nbs1 Connects CDK and ATM to Regulate HR–Mediated Double-Strand Break Repair
PLoS Genetics
·
2013
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257 cit.
·
DOI
8
Doxorubicin Activates ATM-dependent Phosphorylation of Multiple Downstream Targets in Part through the Generation of Reactive Oxygen Species
Journal of Biological Chemistry
·
2004
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253 cit.
·
DOI
9
Interferon‐inducible expression of APOBEC3 editing enzymes in human hepatocytes and inhibition of hepatitis B virus replication†
Hepatology
·
2006
·
249 cit.
·
DOI
10
Impaired Autolysosome Formation Correlates With Lamp-2 Depletion: Role of Apoptosis, Autophagy, and Necrosis in Pancreatitis
Gastroenterology
·
2009
·
241 cit.
·
DOI
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